Osteochondropathy. Aseptic subchondral necrosis (osteochondropathies)
OSTEOCHONDROPATHY [osteochondropathy(Greek, osteon bone + chondros cartilage + pathos suffering, disease); syn.: aseptic necrosis bones, osteochondrolysis, epiphyseal necrosis] - a number of diseases of the osteoarticular apparatus, occurring mainly in childhood and adolescence, occurring in stages and manifested by aseptic necrosis of certain subchondral located most loaded areas of the skeleton, their compression and fragmentation.
Essence of the disease consists of a local disturbance of the blood circulation of the bone and the development of areas of aseptic necrosis. The epiphyses of the long and short bones, vertebral bodies and other spongy bones.
All O. can be divided into 4 groups: O. epiphyses tubular bones- humerus (Hass disease), metacarpal bones, phalanges of the fingers (Tiemann disease), heads femur(see Perthes disease), head II, less often III, metatarsal bone (see Köhler disease); O. short spongy bones - vertebral bodies (see Calve's disease), lunate bone (see Kienbeck's disease), scaphoid bone of the hand (Prizer's disease), scaphoid bone of the foot (see Köhler's disease); O. apophysis (apophysitis) - juvenile apophysitis of the vertebrae (see Scheuermann-Mau disease), apophysitis pelvic bones, tibia(see Osgood-Schlatter disease), kneecap- Larsen-Johansson disease (see Patella), calcaneus(see Haglund-Schinz disease), apophysitis of the fifth metatarsal bone (Islen disease); partial wedge-shaped necrosis of the articular ends of bones (osteochondrosis dissecans) - the head of the humerus, the distal epiphysis of the humerus, the distal epiphysis of the femur (see Koenig disease), the body of the talus (Haglund-Sever disease).
How independent disease O. was first isolated in 1923 by G. Axhausen, then this pathology was described by E. Bergmann in 1927. However, even earlier, in 1910, aseptic necrosis of the femoral head was described by A. Legg ), and in 1924 by G. Pertes.
According to M.V. Volkov (1974), among all orthopedic pathologies, O. is 2.7%. Within this group, according to N. S. Kosinskaya, aseptic necrosis in the hip joint accounts for 34%, knee - 8.5%, elbow - 14.9%, wrist joint and wrists - 42.6%. Damage to the joints and bones of the upper limb is observed in 57.5%, lower limb -42.5% of cases.
Etiology and pathogenesis
The causes of O. are not clear. It is believed that trauma, infection, congenital factors, dysfunction of the endocrine glands, metabolic disorders, etc. are important. Most researchers consider the main etiol, chronic or acute injury in combination with circulatory disorders. M.V. Volkov (1974) believes that changes in the skeleton with O. are a consequence of osteodystrophy of an angioneurogenic nature.
Pathological anatomy
For all types of O., the pathological changes are identical. They consist of dystrophic-necrotic changes in the articular cartilage, circulatory disorders in the area of the epiphyses and in the subchondral parts, various sizes and shapes of foci of necrosis and microfractures of the bone crossbars of the cancellous bone, as well as the reparative reaction of osteochondral elements, combined with the restructuring of these elements. Macroscopically, changes are revealed in the increasing deformation of the epiphyses of the bones, the development of deforming arthrosis, and the appearance of loose articular bodies due to the sequestration of necrotic subchondral fragments. Pathomorphology. features are determined by local anatomical conditions and the degree of mechanical load on the damaged bone organs.
Microscopically, in the subchondral sections, a disordered arrangement of bone crossbars and their fragments, partially fused with endosteal callus, is noted. Many bone fragments are devoid of osteocytes and appear necrotic, clearly standing out against the background of foci of fibrosis, hemorrhages, lumps of fibrin and multicellular newly formed bone substance, which has not yet undergone mineralization and restructuring. Hyaline cartilage of the articular surfaces undergoes focal homogenization, calcification and disintegration, resulting in “exposure” of the articular surfaces with subsequent closure of the defects by fibrous tissue. The dynamics of morphol and changes in the femoral head in Perthes disease have been studied in sufficient detail. The basis of these changes is the primary aseptic infarction of the subchondral parts of the upper outer, most loaded parts of the femoral head. Foci of necrosis have a flat, cone-shaped and rounded shape. The depth of necrosis when the disease is 2-3 years old is from 1 to 3.5 cm. In the circumference of the foci of necrosis during these periods, a kind of demarcation zone appears, represented by skeletogenic or fibrocartilaginous tissue, rich in blood vessels (Fig. 1). In this case, intensive resorption of dead bone material by osteoclasts and its replacement with newly formed bone is noticeable, but complete recovery is observed only with relatively limited lesions. Outside the demarcation zone, there is osteoporosis preceding necrosis (see), traces of fused microfractures, fragmental structures (Fig. 2), foci of fibrosis and eburnation, secondary necrosis, which often end in the formation of a bone cyst. Sequestration of necrotic fragments with the formation of free intra-articular bodies is possible (see Articular mouse), more characteristic of O. of the knee joint (Konig's disease). It is very significant that both in foci of necrosis and in free intra-articular bodies, necrotic bone does not lose its architectonics. A feature of Koenig's disease is a free intra-articular body, which is bone tissue covered with hyaline cartilage. And only in the zone of the former demarcation are visible traces of microfractures, proliferation of chondroid tissue and a formed endplate (Fig. 3). Such changes indicate traumatic genesis articular mice with Koenig's disease. The absence of foci of necrosis is also characteristic of O. tibial tuberosity - Osgood-Schlatter disease. All other varieties of O. are characterized by primary necrotic changes bones characteristic of Perthes disease.
A certain complication of morphological patterns is observed in O. of the apophyses of the vertebrae (Scheuermann-May disease), in which, along with the changes in the cancellous bone described above, a violation of the ossification of the epiphyseal plates, degeneration of the intervertebral discs with the formation of hernial protrusions of cartilage into the medullary spaces (hernia) are noted Schmorl). The flattening of the vertebral body, characteristic of Calve's disease, is caused by a decrease in the strength of the beam structures against the background of ongoing mechanical load.
Pathological studies indicate that O. of any localization can have a different nature. The embolic (vascular) origin of foci of aseptic necrosis is supported by their development during decompression sickness, described in diving fishermen. I. V. Shumada et al. (1980) showed in an experiment that aseptic bone necrosis occurs with dyscirculatory disorders combined with increased function and load on the bone. Numerous reports have been published on aseptic bone necrosis arising in connection with metabolic disorders in long-term use corticosteroids, for example, after kidney transplantation. In this case, nephrogenic osteopathy, caused by hron, kidney disease, is also important (see Nephrogenic osteopathy).
Clinical picture
The course of O. is usually long-term (2-3 years). D. G. Rokhlin (1952) distinguishes 3 phases wedge, the course of aseptic necrosis: the necrosis phase, the degenerative-productive phase, or the fragmentation phase, and the outcome phase. In the first phase, the patient complains of fatigue, vague painful sensations; small functions, disturbances, local pain, lameness appear (if the lower extremities are affected), then compression of the necrotic area of the bone occurs. In the second phase, the pain intensifies, the patient spares the affected limb. By the end of the second phase, the pain may disappear, but the function of the limb is not restored. In the third phase, a recovery process or the development of deforming arthrosis with the resumption of pain is observed.
In children during the growth period, aseptic necrosis leads to a violation of osteogenesis - inhibition of enchondral ossification. With the development of secondary ischemic disorders, premature closure of the growth plate and deformation of the articular end of the bone are observed.
Diagnosis
The decisive role in diagnosis is played by rentgenol, research. As a rule, radiography of the affected segment is performed in standard projections, and, if necessary, tomography (see). Radiologically, 5 phases, or stages, can be conventionally distinguished in O.’s development. In stage I - subchondral necrosis - rentgenol, the picture of the bone may not be changed, despite the presence of symptoms of the disease; at the end of the stage, a weak limited compaction of the bone substance appears in the area of necrosis. In stage II - the stage of a compression fracture - in the zone of necrosis, an area of bone compaction of a homogeneous or uneven nature is visible on the x-ray. The joint space is widened. Stages I and II correspond to the necrosis phase. In stage III - the stage of resorption - the affected area consists of several dense structureless fragments irregular shape(fragmentation phase). Stage IV - the stage of regeneration - is characterized by gradual normalization of rentgenol, bone structure, sometimes with the development of cystic cavities. In the final, V stage of O., either complete restoration of the structure and shape of the bone occurs, or signs of deforming arthrosis develop (see). Stages IV and V correspond to the outcome phase. The intervals between regular rentgenol examinations depend on the stages of the disease and average from one to several months in stage II, from 0.5 to 1 year, and sometimes more, in stages III and IV.
Treatment and Prognosis
Treatment of aseptic necrosis of the epiphyses of bones in children due to high reparative capabilities during the growth period should be conservative, with unloading of the affected limb and the use of physiotherapeutic procedures. If O. in children and adults ends in deformation of the articular end, in some cases it is indicated surgery: corrective osteotomies (see), arthroplasty (see), etc.
The prognosis for life is favorable. O.'s prognosis for restoration of limb function is determined by the timeliness of treatment started. Self-healing is rare. Due to late or irrational treatment full recovery bone shape and function of the limb usually does not occur - consequences in the form of arthrosis remain.
Bibliography: Volkov M. V. Bone diseases in children, M., 1974; Kosinskaya N. S. Degenerative-dystrophic lesions of the osteoarticular apparatus, JI., 1961; Multi-volume guide to orthopedics and traumatology, ed. N. P. Novachenko and D. A. Novozhilova, vol. 1, p. 516, M., 1967; Multi-volume guide to pathological anatomy, ed. A. I. Strukova, vol. 6, p. 60, M., 1962; Revenko T. A., Astakhova E. I. and Novichkova V. G. On the etiology of aseptic necrosis of the femoral head in adults, Orthop, and traumat.. No. 10, p. 38, 1978; Reinberg S. A. X-ray diagnosis of diseases of bones and joints, book. 1-2, M., 1964; P u b a w e v a A. E. Private X-ray diagnostics of diseases of bones and joints, p. 57 and others, Kyiv, 1967; Startseva I. A. and JI e n s k i y V. M. Morphological changes with aseptic necrosis of the femoral heads in adults, Orthop, i travmat., No. 12, p. 56* 1977; Sh u m a d a I. V. et al. About aseptic necrosis and racemose reconstruction of the epiphyses of bones in adults, in the same place, No. 7, p. 33, 1980; In e 1 in M. Histological differential diagnosis of aseptic bone-necrosis, Acta morph. Acad. Sci. hung., v. 27, old 95, 1979; Campbell's operative orthopedics, ed. by J. Speed, v. 11, p. 1171, L., 1956; Colas M., S a r r e t J. P. e t F i-s with h e r L. Contribution a Petude de la vascularisation intraosseuse de 1 "astragale, Bull. Ass. Anat. (Nancy), t. 59, p. 819, 1975; E d e i k e n I. a. Hodes P. Roentgen diagnosis of diseases of bone, Baltimore, 1973; Lichtenstein L. Diseases of bone and joints, St. Louis, 1975; M e 1 s e n F. a. Nielsen H. E. Osteonecrosis following renal allotransplantation, Acta path, microbiol. scand., v. 85A, p. 99, 1977; Orthopedic surgery and traumatology, ed. by J. Delchef a. o., p. 438, Amsterdam, 1972; P u 1 s P. Die Primarlasion und Pathogenese der idiopathischen Hiiftkopfnekrose, Z. Rheumatol., Bd 35, S. 269, 1976; Wade S. E. a. o. Incidence of dysbaric osteonecrosis in Hawaii's diving fishermen, Undersea Biomed. Res., v. 5, p. 137, 1978.
E.P. Mezhenina; N. K. Permyakov (pat. an.), V. V. Kitaev (rent.).
Osteochondropathy (synonym: aseptic bone necrosis, apophysitis) is a disease of the epiphyses and apophyses of bones, occurring in childhood and adolescence. Most often the head of the femur is affected (see), the tibial tuberosity, the heads of the metatarsal bones, the vertebral bodies and, less commonly, other bones. Osteochondropathy is manifested by pain and often swelling in the affected area. The diagnosis is usually made by X-ray examination. It is favorable for osteochondropathy, but if treated incorrectly, this disease can cause the development of arthrosis (see).
Osteochondropathia (osteochondropathia; from the Greek osteon - bone, chondros - cartilage and pathos - suffering, disease; synonym: aseptic necrosis of bone, epiphysionecrosis, apophysitis) - group pathological processes, characterized by a peculiar change in the spongy substance of short and epiphyses of long tubular bones, often combined with changes in the articular cartilage and ending in deformation of the affected bone.
Etiology and pathogenesis. Osteochondropathy occurs as a result of local malnutrition of the bone, the causes of which, apparently, are different depending on different localizations process (overload, microtrauma, etc.).
Osteochondropathy has a certain phase course. The process is based on spontaneously occurring aseptic subchondral necrosis bone tissue(Phase I), complicated by a secondary pathological depressed fracture of the necrotic area (Phase II, impression fracture). Adjacent connective tissue(articular and growth cartilages, joint capsule, periosteum, ligaments) participates in the resorption of necrosis and the replacement of its elements with osteoid substance (phase III, phase of resorption, fragmentation), which then ossifies. As a result, the bone structure of the affected area is restored (phase IV, recovery phase) and osteochondropathy spontaneously ends, but with varying degrees of deformation of the affected area (phase V, final). If this deformation is significant, the articular end of the adjacent bone of this joint is correspondingly and gradually modeled, deforming; This is how a deforming process (arthrosis) can gradually arise - a common complication of osteochondropathy. Almost individual phases are partially superimposed in time on one another.
There are certain skeletal bones and typical places in these bones (covered with cartilage) to localize osteochondropathy. In literature various localizations Osteochondropathies are often (and not always accurately) designated by the names of the authors who first described them. Thus, osteochondropathy of the pubosciatic joint is called Van Neck disease, the vertebral body - Calve's disease, the navicular bone of the foot - Köhler's disease I, the heads of the metatarsal bones - Köhler's disease II, the lunate bone of the carpus - Kienbeck's disease, the femoral head - Perthes or Legg's disease - Calve-Perthes disease (see Perthes disease), tibial tuberosity - Osgood-Schlatter disease (see Schlatter disease), scaphoid bone of the wrist - Praiser's disease, sesamoid bone of the first metatarsophalangeal joint - Renander-Muller disease, sternal end of the clavicle - disease Friedrich, the ossification nucleus of the calcaneus - Haglund-Schinz disease, the apophyses of the vertebral bodies - Scheuermann-May disease, the medial femoral condyle, as well as the capitate eminence of the humerus - Koenig disease. Some authors also classify changes in the shape of the vertebrae as osteochondropathy - Kümmel's disease. The diagnostic conclusion cannot be limited to a short phrase, for example, “Köhler’s disease II”; It is also necessary to determine the phase of the disease, on which certain medical and labor prescriptions and restrictions depend.
The pathological anatomy of osteochondropathy has been studied using specimens obtained during operations. The essence of pathological changes is the same for all diseases belonging to the group of osteochondropathy.
The initial stages of the disease have not been studied, since operations for osteochondropathy are performed in late stages. At the height of the disease, deformation of the affected part of the bone or the entire bone is macroscopically expressed when the process is localized in small bones. With Calvet disease, the vertebra is flattened, sometimes more in the posterior part. With Perthes disease, the femoral head flattens; Bone thickenings in the form of ridges form along its edges. In Köhler disease I, the navicular bone of the foot is flattened (Fig. 1). In Köhler disease II, the heads of the affected metatarsal bones become flattened. With Kümmel's disease, the affected vertebrae decrease in height, take on a wedge-shaped shape, and become rarefied. With Osgood-Schlatter disease, the area of the tibial tuberosity is deformed. In Koenig's disease (osteochondritis dissecans), a section of the medial femoral condyle is torn away over time and is located in the joint cavity in the form of a free articular body - a section of spongy bone covered with articular cartilage. Along the line of separation from the bone there is a narrow zone fibrous tissue. In the bone part of the fragment one can see microcalluses that solder the broken beams. IN long bones and small bones of the hands and feet, the main changes are localized in the subchondral zones. Microscopically, randomly arranged small bone fragments are visible here, representing fragments of bone beams; osteocytes do not stain in them. There are also fragments of cartilage with dystrophic changes, and sometimes with proliferation of cartilage cells. Structureless protein masses lie in the same zone (Fig. 2). Some of them are formed, apparently, by compacted fibrin, some are the main substance of cartilage. Granular deposits of lime precipitate into these structureless masses, which are sometimes incorrectly mistaken for bone decay ( bone flour). In the bone beams one can detect traces of former fractures: individual beams are welded together by microcalluses; there are areas of newly formed bone substance into which old bone beams, devoid of osteocytes, are soldered. Sometimes the newly formed bone substance has the character of an osteoid.
Rice. 1. Deformation of the scaphoid bone.
Rice. 2. Protein masses in the interosseous spaces.
The sequence of pathological changes in osteochondropathy is interpreted in two ways. Some believe that the basis of osteochondropathy is primary aseptic necrosis of bone beams with subsequent fractures and sometimes fracture of the entire bone. Others classify osteochondropathy as a microtraumatic disease: microfractures of bone beams primarily occur, their fusion occurs under conditions of ongoing functional load, so healing is incomplete and is accompanied by the development of deformities. See also Bone tissue ( pathological anatomy). T. Vinogradova.
Clinical picture and symptoms. Osteochondropathy is a disease of a growing organism and is observed mainly in children, adolescents and young men, less often in infants and only in some localizations in blooming age. The onset of the disease is mostly inconspicuous and gradual. Leading clinical signs are strictly localized pains that intensify with load and cause sparing of this section, restriction of movements in it, as well as pain when pressure is applied to the affected section and along the long axis of the bone; Local swelling and even hyperemia are common. Fever, changes in peripheral blood, edema abscesses and fistulas are absent.
Confident diagnosis and differential diagnosis possible only on the basis of radiological data. It is necessary to differentiate osteochondropathy depending on the location from tuberculosis, fracture, zone of restructuring, nonspecific arthritis, rickets, decompression sickness, etc. It is necessary to take into account that a number of bone diseases (tuberculosis, eosinophilic granuloma, etc.) can be complicated by osteochondropathy.
The prognosis for osteochondropathy is favorable, since the disease ends spontaneously. To prevent an increase in the volume of necrosis and the degree of pathological depression of the bone, it is advisable to unload the affected area in phases 1-II-III of the disease; this facilitates repair and more perfect restoration of bone shape in phase IV osteochondropathy.
When examining the skeleton for other reasons, sometimes it is possible to identify changes on radiographs that are typical of the consequences of osteochondropathy that was once suffered and not noticed by the patient. It is also not uncommon for people to seek help only with complaints of osteoarthritis that has arisen as a result of unnoticed osteochondropathy.
Osteochondropathy of the vertebral body (Calvé's disease, flat, osteonecrotic vertebra) occurs in infants, children and adolescents in the thoracic, lumbar or cervical spine; at the level of slight angular kyphosis, radiographic evidence reveals a progressive collapse of the body of one vertebra to 1/2 - 1/4 or more of the usual height, more in the front, with a slight protrusion anterior section. The intensity of the shadow of the affected vertebra is increased due to necrosis and pathological compression. The height of adjacent intervertebral spaces is often increased. Over the course of several years, the height of the affected vertebra (usually incomplete) and the normal pattern of its shadow on radiographs are restored.
Osteochondropathy of the navicular bone of the foot (Köhler's disease I) affects infants, children and adolescents, much more often boys. On radiographs, the shadow of the ossification nucleus of the scaphoid bone in phase II becomes thinner and darkened, and both adjacent joint spaces widen. IN III phase the core shadow fragments and then recovers without treatment.
Osteochondropathy of the head of the II, less often the III - IV metatarsal bones (Köhler's disease II) is associated with increased loading of the metatarsus (flat feet). Solitary, less often multiple, lesions are observed in adolescents and people young, more often in women. In phase II, the affected head flattens and thickens, and the adjacent joint space widens. In phase III, the head looks as if it consists of separate fragments. The darkening and unevenness of the shadow of the head disappears in phase IV, which usually ends spontaneously no later than the third year of the disease. The gap of the adjacent metatarsophalangeal joint remains widened forever; the base of the adjacent phalanx is modeled according to the head of the metatarsal bone. In phase V, various degrees of deformation of the head are possible - from barely noticeable to very rough with osteophytes.
Osteochondropathy of the lunate bone of the wrist (Kienböck's disease) is typical for people aged 15-30 years who heavily load the wrist. The peculiarity of this localization of osteochondropathy is the duration (up to 2 years or more) of phase I of the disease, i.e., the phase of negative radiological data, which, with insufficient consideration of local clinical events and profession often raises unjustified suspicions of simulation. The flattening, deformation and compaction of the bone in phase II are replaced by the unevenness of its shadow in phase III and homogenization in phase IV, but without restoration of the original shape and size of the bone by the end of the disease.
For a very rare osteochondropathy of one, usually the medial, of the sesamoid bones of the first metatarsophalangeal joint (Renander-Müller disease), the X-ray clinical picture of the disease in dynamics is also typical, but without restoration of the normal shape and size of the affected bone by the end of the disease.
Osteochondropathy of the nucleus (nuclei) of ossification of the tubercle of the calcaneus (Haglund-Schinz disease) is very rare and has not been histologically proven. Characteristic of children and adolescents. Convincing arguments in favor of the presence of this disease are the clear displacement of I from the fragments of the ossification nucleus of the tubercle and the thickening of the cartilaginous layer, transparent to x-rays, between the nucleus and the calcaneal bone mass.
Scheuermann and May (N. Scheuermann, S. May) described a disease of the thoracic spine in adolescence and early adolescence, more often in men, as osteochondropathy of the vertebral apophyses (Scheuermann-May disease), as the cause of the so-called juvenile kyphosis. The basis was X-ray picture changes in the apophyses of the vertebrae, similar to osteochondropathy, but not histologically proven. Some authors attribute changes in juvenile kyphosis to chronic injury apophyses when the spine is overloaded with the development of anterior cartilaginous hernias and subsequent deformities. Local pain is rare and not intense. Radiologically, in dynamics, single or multiple unevenness of the platforms of the bodies of the affected thoracic, less often upper lumbar, vertebrae (caused by cartilaginous herniations of intervertebral discs), their retardation in height, the formation of kyphosis here, and later - thinning of the discs are observed. Subsequently, irreversible deformative and degenerative changes (osteochondrosis) usually develop at this level.
Occasionally, in adulthood, due to injuries suffered, usually in the femoral head, late osteochondropathy occurs, the dynamics of which are characterized by the absence of a recovery phase and the repetition of the first three phases. The prognosis is unfavorable due to progressive destruction of the femoral head.
One of the varieties of aseptic osteonecrosis - Koenig's disease [synonym: partial wedge-shaped osteochondropathy of the articular surface, dissecting osteochondrosis (osteochondrosis dissecans)] - consists in the gradual delimitation of the necrotic fragment from the surrounding living bone by granulations, and then in its rejection through the articular cartilage into the joint cavity, where it becomes a “joint mouse”, sometimes being pinched. The classic and most common localizations of this type of osteochondropathy are the articular surface of the medial femoral condyle, the capitate eminence of the humerus and the trochlea of the talus, rarely other parts of the skeleton.
Osteochondropathies are quite rare degenerative diseases of the joints, which are based on aseptic subchondral necrosis of the spongy substance of the epiphyses with subsequent deformation of the articular end (head) of the bone. Thus, this is a primary bone form of degenerative-dystrophic joint lesions. Osteochondropathy as an independent nosological form was first described by Axhausen (1923).
Various forms of osteochondropathy occur mainly in children and young men. The course of the disease at this age is favorable, which is explained by the good reparative reactions of articular cartilage. In adults, subchondral osteonecrosis is much less common, but due to less advanced reparative processes it is more severe, resulting in deforming arthrosis.
The etiology and pathogenesis of osteochondropathy have not been fully established. Most authors consider the cause of focal necrosis of the epiphysis to be a violation of the blood circulation of this part of the bone. Axhausen (1928) considered aseptic subchondral osteonecrosis as a bone infarction followed by necrosis of part of the epiphysis and sequestration of a bone fragment.
He considered the possible cause of this infarction to be an embolism of the artery supplying the epiphysis. However, the presence of osteochondropathy organic damage or arterial blockage was not observed by anyone. In this regard, it has been suggested that it is not blockage that occurs, but vasomotor disturbances of arterioles such as paralysis or spasm, which are based on a violation of the central regulation of vascular tone.
The subsequently developing venous spasm worsens the process both due to the histochemical changes it causes and because it is additional irritating factor(Vezet). Leriche, Hamant and Bodart, Bentzen, Lombard suggest that this vasomotor reaction occurs as a result of mechanical injury to the joint (occupational, sports or accidental).
“Diseases of the joints”, M.G. Ostapenko, E.G. Pihlak
In the first stage of the disease, necrosis of the spongy substance of the epiphysis is observed in its part located directly under the articular cartilage, in the so-called support zone, i.e., in the place of greatest load. Subsequently, the necrotic area of the bone is separated, forming a sequestrum, which always remains adjacent to the “niche” formed in the epiphysis. When osteonecrosis develops in children, cartilage damage is never observed,…
With osteochondropathy of the vertebral body (Calvé's disease), a flattening of this vertebra (most often one of the thoracic vertebrae) occurs, which quickly, sometimes within several weeks, turns into a dense, thin plate. This is followed by restoration of the vertebra through its growth, since the upper and lower growth zones remain intact. Clinic and radiological picture of Calve's disease in initial stage extremely reminiscent of tuberculosis...
Movements in the hip joint are somewhat limited, and painful limitation of abduction and rotation of the limb is characteristic, while flexion and extension of the hip continue to remain free. When tapping in the area of the greater trochanter and femoral head, slight pain is noted. Due to thickening and deformation of the head and shortening of the femoral neck, the affected leg is sometimes shortened. Atrophy of the muscles of the limbs or any other trophic...
A severe case of Perthes disease in a 12-year-old boy. Extensive subchondral necrosis of the femoral head. In the outcome phase, the disappearance of the sequestrum and the remaining deformation of the head and socket without the development of growths are observed, how this disease differs from deforming osteoarthritis. In addition, the joint space is preserved, and in some cases even remains widened, for many years. In some patients, through...
Second Köhler's disease in a 14-year-old girl. A bone sequestration is clearly visible in the head of the second metatarsal bone of the left foot. Aseptic subchondral osteonecrosis in adults has clinical and pathological features compared with osteonecrosis in children. These features primarily consist in the absence of compensatory hyperplasia articular cartilage and usual for childhood recovery reactions. In view of this, the Soviet...
The joint “mouse” almost never resolves, causing a kind of “joint blockade” clinic. There may even be an increase in the size of the joint “mouse” and calcification of the cartilage tissue present in it. The defect in the epiphysis bone is gradually replaced by newly formed bone and disappears, although this section of the bone head remains flattened. With the long-term existence of an articular “mouse”, damage to the articular cartilage occurs, resulting in...
X-rays of the joints reveal a typical picture of a bone niche in the upper pole of the head with the presence of a sequester in it. In the future, some narrowing of the joint space (cartilage degeneration), characteristic deformation of the head and acetabulum and the development of secondary deforming arthrosis (as opposed to Perthes disease) may occur. General state patients, temperature and blood picture are the same as...
Koenig's disease clinically occurs in two phases. In the first phase, only slight vague pain is observed. In rare cases, mild synovitis develops with the greatest effusion. However, with careful examination, a positive Axhausen sign can be detected: when pressure is placed on a strictly localized area of the internal condyle (outside of the patella) and at the same time bending the leg at the knee, severe pain occurs….
The diagnosis of osteochondropathy at an early stage is difficult due to the very vague clinical picture. The reference points for diagnosis are unilateral lesions without signs inflammatory process(absence of exudative phenomena, significant pain on palpation, skin hyperemia and increased skin temperature, normal blood counts, etc.), as well as a typical x-ray picture (characteristic deformation of the head with the appearance of sequestration with normal or...
Coste, Massiar, Chatelon (1961) believe that various mechanical factors only favor the development of the disease, but the main thing is vascular factor. In most of the patients they observed, subchondral necrosis appeared during and after various diseases occurring with a vascular component (conjunctivitis, allergic diseases, protein shock, etc.). In addition, the authors attach importance to the exchange factor, and...
a pathological process characterized by necrosis of a section of bone in that part of the skeleton that undergoes significant loads. Primary A.n.c. (osteochondropathies) are observed during the period of growth of the body, i.e. in childhood and adolescence. They are based on subchondral avascular necrosis of bone and bone marrow. In this case, cartilage is not damaged, so ankylosis never occurs. Osteochondropathies are relatively benign with restoration of bone tissue and a favorable outcome. They should be distinguished from secondary A.n.c. in rheumatic diseases, when simultaneous or sequential damage to cartilage occurs (due to the growth of pannus or degenerative changes with subsequent destruction). For example, with aseptic necrosis of the femoral head, there is often protrusion of the acetabulum of the innominate bone, which is not observed in osteochondropathy. There are osteochondropathy of the head of the femur (Legg-Calvé-Perthes disease), the heads of the metatarsal bones, usually the second and third (Köhler's disease II), the navicular bone of the foot (Köhler's disease I), the lunate bone of the hand (Kienbeck's disease), the phalanges of the fingers (Köhler's disease Thiemann), scaphoid bone of the hand (Preiser's disease), vertebral body (Calvé's disease), sesamoid bone of the first metatarsophalangeal joint, tibial tuberosity (Osgood-Schlatter disease), calcaneal tuberosity (Haglund-Schinz disease), body of the talus (Haglund disease ), apophyses of the vertebrae (Scheuermann-Mau disease) of the patella (Larsen-Johansson disease), partial (wedge-shaped) osteochondropathy of the articular ends of the distal epiphyses of the humerus and femur (Konig disease). For rheumatic diseases (rheumatoid arthritis, SLE, systemic scleroderma, osteoarthritis), aseptic necrosis of the femoral heads is usually observed, much less often - the heads humerus, elbow and radius, even more rarely the bones of the lower leg and wrists.
Etiology and pathogenesis. According to most researchers, the main cause of osteochondropathy is trauma combined with impaired local circulation, leading to ischemia of the corresponding areas of the bone. In the emergence of A.n.c. In rheumatic diseases, vascular changes also play an important role. It is believed that in this case there is damage to intraosseous vessels of an immune, in particular immunocomplex nature (i.e., one of the manifestations of vasculitis occurs). Facts such as thrombosis or fat embolism of the vessels of the epiphyses of bones are also of certain importance. The negative role of glucocorticosteroids used in treatment turned out to be exaggerated, since A.n.c. often occurred in patients who had never taken them. A.n.k. observed with decompression sickness, alcoholism, radiation, hemoglobinopathies (sickle cell anemia). Among osteochondropathy, the most common diseases are Legg-Calvé-Perthes, Osgood-Schlatter, Scheuermann-Mau diseases, and less frequently Köhler, Koenig, and Kienbeck diseases.
Osteochondropathy of the femoral head (primary aseptic subchondral necrosis, Legg-Calvé-Perthes disease).
The disease occurs mainly in children aged 5-12 years, less often in earlier or later periods. Clinical picture. The disease has several stages, characterized by anatomical and radiological changes. In the first stage (initial stage of necrosis), a histological picture of focal necrosis of bone and bone marrow is observed. There are no changes in radiographs during this period. In the second stage (compression fracture stage), which develops several months from the onset of the disease, compression of the dead bone area is detected due to fractures of the bone beams and the restructuring of the surrounding bone tissue. The epiphysis of the femur decreases and becomes deformed. On radiographs, this is manifested by thickening of the bone shadow and an increase in the joint space. In the third stage (resorption stage), resorption of necrotic bone occurs. On the radiograph, the shadow of the head appears to be broken into several isolated structureless fragments. After 1.5-3 years, the disease transitions to the fourth stage (repair stage). Newly formed bone tissue replaces necrotic areas of bone. The process lasts 1-2 years. Sequestration-like shadows disappear on radiographs. And in the last fifth stage, the structure and shape of the head is restored
femur. With incomplete repair, conditions are created for the development of secondary arthrosis. Aseptic necrosis of the femoral head in rheumatic diseases early stages It has
a similar radiological picture; in addition, there are characteristic signs of coxitis: osteoporosis, narrowing of the joint space, cystic clearings and bone erosions (especially with rheumatoid arthritis). The defeat is often bilateral. A feature of the process is very slow and incomplete repair or (more often) its absence.
Clinical picture. Usually, after an injury or awkward movement, unstable local pain(initially when moving), sometimes lameness. The pain often radiates to groin area, hip, knee joint. Pain appears during rotation and abduction of the hip, lameness increases, and the function of the limb is gradually impaired (significantly in the later stages). The affected limb is shortened by several centimeters. A positive Trendelenburg sign is noted: when standing
on the affected leg, the femoral-gluteal fold of the unaffected side falls below a similar fold of the opposite side. Often pain bothers the patient 1-2 years before the first radiographic changes appear. Often there is some discrepancy between the clinical picture and radiological changes: at an early stage there may be sharp pains and significant disturbance of gait, and as compression fractures develop, leading to severe deformation of the femoral head, pain temporarily decreases, while there is a significant limitation in hip abduction and rotation.
Diagnosis. The main thing in making a diagnosis is the characteristic x-ray picture. However, at the first stage, the disease is not diagnosed radiographically. The possibilities of nuclear magnetic resonance for diagnosing avascular necrosis at an early stage are currently being studied. For rheumatic diseases A.n.c. are always complications, and therefore their diagnosis after establishing the underlying disease is not difficult.
Differential diagnosis carried out with tuberculous coxitis. With the latter, there is also pain, flexion contractures and signs of destruction of the femoral head on radiographs, there is a significant increase in the hip joint, the formation of subcutaneous abscesses and fistulas with serous purulent discharge (odorless). The presence of neuropathic arthropathy (see) is assumed in cases where there are significant radiographic changes joint in the absence of pain.
Treatment. The main thing in the treatment of secondary A.N.C. should be considered active therapy of the underlying disease, preventing the emergence of conditions for the development of aseptic necrosis (coxitis, immune complex vasculitis). Once the diagnosis has been made, it is necessary to free the affected limb as much as possible from physical activity(walking with a cane or crutches). Prescribed drugs that improve microcirculation processes (complamin, prodectin, etc.). Good results obtained by prescribing repeated courses of calcitrin (thyrocalcitonin), a hormonal drug obtained from the thyroid glands of animals. It prevents resorption and stimulates the deposition of calcium and phosphorus in bone tissue. Before starting treatment, a test is performed (1 unit of calcitrin in 0.1 ml of solvent is injected intradermally). If well tolerated, the drug is prescribed in a dose of 3-5 units intramuscularly, daily for 1-1.5 months or every other day for 2-3 months. Repeated courses are possible no earlier than after 2 months. At the same time, calcium preparations (calcium gluconate - 3-4 g per day), sodium fluoride (coreberon, etc.) 0.025 g 3 times a day and vitamin D2 (ergocalciferol) 1000-5000 units per day are prescribed for a long time (for years). Prescribe anabolic drugs (retabolil, nerobolil) repeated courses. Physiotherapy (electro- and phonophoresis, laser therapy, microwave therapy). The issue of using anticoagulants and antiplatelet agents in the treatment of these patients was discussed, but they did not find wide application. Exercise therapy is carried out only in conditions of reducing the load on the affected joint. From surgical methods in the early stages, osteotomy is used, in the later stages, endoprosthetics and arthroplasty are used.
Aseptic necrosis of the tibial tubercle (Osgood-Schlatter disease)
the disease occurs predominantly in adolescence (usually under 18 years of age); often bilateral. Patients are concerned about pain in the area of the tibial tuberosity, especially when walking; Palpation reveals a painful swelling in this area. On a radiograph in the lateral projection in the area of the tibial tuberosity, areas of clearing are visible, alternating with areas of darkening; sometimes there is complete fragmentation of the tuberosity. The disease lasts 0.5-1.5 years and usually ends with complete recovery.
Treatment. In case of pain - rest, subsequently limiting exercise, physiotherapy.
Spinal osteochondropathy (Scheuermann-May disease)
aseptic necrosis of the apophyses of the vertebral bodies.
Clinical picture. The disease begins in adolescence. Initially, the concern is a slight pain in the spine, often of a diffuse nature, intensifying after exercise and disappearing after a night's rest; An arched curvature of the spine (kyphosis) gradually develops. Often there is a rough crunch in the spine when the body is tilted forward. Later, radicular pain occurs.
Diagnosis. The correct diagnosis can be made by a characteristic X-ray picture of the spine, especially in the lateral projection: the vertebral bodies are wedge-shaped, their anterior sections are located lower than the posterior ones; Unlike Calvet's disease, several vertebrae are affected. Differential diagnosis is carried out with osteomyelitis, spinal tuberculosis.
Treatment. The main role is given to exercise therapy and orthopedic measures. If radicular syndrome occurs, treatment is usually inpatient (traction, back muscle massage, physiotherapy). With an unfavorable course, osteochondrosis develops.
Aseptic necrosis epiphysis of the femur (Konig's disease). In these cases, the distal epiphysis of the femur is most often affected.
Clinical picture. Initially, pain (intermittent) in one, less often in both knee joints bothers you; then the pain becomes constant and intensifies when walking. Often there is a secondary
Clinically, in this group of diseases, relatively small changes in the objective condition of patients at the onset of the disease are natural, and only with already pronounced changes do pain, dysfunction, and swelling of the periarticular tissues appear.
Radiologically, the alternation of several stages of the disease is natural. In the initial stage, a slight violation of the bone structure is determined, similar to small-spotted osteoporosis, alternating with areas of compaction of bone tissue.
In the subchondral zones, multiple small compression fractures, as a result of which the bone structure becomes denser, the end plates become tuberous, and the joint spaces widen. In later stages, necrotic bone beams resolve and normal ones are restored. A motley picture of rarefaction and compaction appears against the background of a coarse trabecular bone structure.
In the final stage, the bone structure is restored, but the shape of the bone remains changed. Subsequently, degenerative-dystrophic changes such as osteoarthritis develop. The joint space may remain widened.
Alban Köhler disease I is a disease characterized by the development of aseptic necrosis of the epiphysis of the navicular bone of the foot, manifested by painful swelling of the foot in this area. It is observed in children aged 4–10 years.
Anteroposterior flattening of the bone, compaction and deformation of it are determined, the contours of the bone are uneven but clear, the joint spaces are not changed or widened. In the fragmentation stage, the bone is divided into 2–3 parts with fuzzy outlines. Over time, the bone gradually acquires a homogeneous structure, and its shape becomes normal.
Alban Köhler II disease is a disease characterized by the development of aseptic necrosis of the head of the 2nd, less often the 3rd or 4th metatarsal bone. It manifests itself as pain in the forefoot, limitation of movements and shortening of the corresponding toe. It occurs more often in girls during adolescence.
The X-ray picture varies depending on the stage of the disease. Initially, there is noticeable flattening of the most convex part of the head and thickening of this part, the appearance of subchondral foci of clearing, and the joint spaces are widened. Then the foci of clearing increase, the head becomes deformed and grows in width, and periosteal layers appear. In the repair stage, a saucer-shaped deformation of the head is noted, and in the outcome stage, deforming arthrosis is noted.
Koenig's disease is a disease of traumatic origin, characterized by subchondral aseptic necrosis of a limited area of the articular surface of the bone with subsequent loss of an osteochondral fragment into the joint cavity. It is observed mainly in men aged 15–30 years who are involved in heavy physical labor. It usually affects one bone, sometimes several or symmetrically located bones involved in the formation of larger and more loaded joints, such as the knee, hip, elbow, etc. The most common site of localization is the internal condyle of the femur.
In the first stage, which begins imperceptibly, a necrotic focus is formed, which is then delimited from healthy tissue and remains in the bone bed for some time. At this time, the radiograph reveals a clearly demarcated, intense shadow of an oblong or oval shape, 0.5–1´1´1.5 cm in size, surrounded by a light rim. When a fragment is moved into the joint cavity, an articular “mouse” is formed, which can lead to periodic blockade of the joint, accompanied by severe pain when moving. On an x-ray, the bone niche on the articular surface appears empty, and a bone fragment is revealed in the joint cavity. A few years later, deforming arthrosis develops.
Kienbeck's disease is a disease of unknown etiology, characterized by the development of aseptic necrosis of the lunate bone of the wrist. It manifests itself as pain in the area of the wrist joint, swelling on the dorsum of the hand.
The X-ray picture depends on the stage of the disease: 1) there are no changes within 3–5 months; 2) bone intensity increases and its volume decreases; 3) fragmentation appears, heterogeneous structure shadows; 4) flattening and further deformation of the bone are observed; 5) deforming arthrosis and sometimes slight subluxation of the bone are noted.
Kümmel disease is post-traumatic aseptic necrosis of the vertebral body, leading to its deformation in the form of a wedge or plate.
Fractures of the upper or lower plate of the body and microfractures of the spongy layer of the vertebral body with hemorrhages are observed, followed by necrosis of the bone beams. There are 3 stages: 1st - immediately after the injury there is severe pain in the area of the bruise for several days or weeks. The X-ray picture is normal, the fracture is not detected and there are no structural changes. At the 2nd stage, a clear period begins, during which the patient either does not complain at all or they are very minor. The duration of this stage is from several weeks to 2 years (on average from 4 to 8 months). X-ray this stage is also asymptomatic. At stage 3, pain appears again. On the radiograph, the affected vertebra is flattened, has the shape of a wedge, with the apex facing anteriorly, or a lateral wedge. The vertebra can also be in the form of a plano-concave lens, with its anterior edge protruding anteriorly, beyond the border of the vertebral bodies adjacent to it. The superior and inferior contours of the damaged vertebral body are usually sharply emphasized due to calcification of the cartilaginous endplates. The structure of the vertebra is not changed, only slight sclerosis is observed at the stage of repair. Intervertebral discs between the affected vertebra and its neighbors are most often unchanged.
As a rule, one vertebra is affected, and only as an exception, two or more. A tomogram has great diagnostic capabilities. On a tomogram in stage I, it is always possible to see cracks in the vertebral body or the penetration of a cartilaginous disc into its spongy structure, and in stage II - rarefication of the spongy substance.
Calvet disease is a disease of unknown etiology, characterized by the development of aseptic necrosis of the body of one of the vertebrae, most often the lower thoracic or upper lumbar. It is observed at the age of 2–15 years.
Characterized by uniform flattening of the vertebral body with simultaneous elongation in anteroposterior size. The contours of the vertebral body are clear and sharp, its shadow is compacted, the bone beams are not visible, the intervertebral spaces are widened. The lateral radiograph shows slight angular kyphosis at the level of the affected vertebra. In the outcome stage, a deformity in the form of a fish vertebra is observed.
Legg-Calvé-Perthes disease is aseptic necrosis of the head of the femur, usually unilateral, occurring predominantly in boys aged 6–10 years. Manifested by limping, limited abduction and extension, pain when moving the hip.
Early radiological sign- the appearance of usuration in the neck of the femur (at the site of attachment of the articular capsule) and then in the fossa of its head, as well as at the border of the epiphysis and metaphysis. Next, an impression fracture of the femoral head develops, flattening of the head, a decrease in height and an increase in its intensity, and expansion of the joint space. During the fragmentation stage, fragments of varying densities appear, resembling sequesters. Further flattening of the head, shortening and thickening of the femoral neck are noted. In the recovery stage there are cystic clearings, then complete repair of the bone structure. The outcome stage ends with deforming arthrosis. There are no ankylosis.
Osgood-Schlatter disease - aseptic necrosis of the tibial tuberosity, occurs more often in boys 13–16 years old. It manifests itself as swelling and pain in this area.
X-ray examination reveals sequester-like fragmentation of the tuberosity. The contours of the bone in this area are eroded. On the anterior contour of the bone, zones of clearing with unclear contours are noted. In the outcome stage, restoration of the bone structure of the tuberosity occurs.
Scheuermann-Mau disease (adolescent kyphosis, juvenile kyphosis) is aseptic necrosis of the apophyses of the thoracic bodies, mainly of the VII–IX vertebrae. It develops slowly and ends with the development of persistent kyphosis (“round” back) in the thoracic region. X-rays reveal disturbances in the ossification of the apophyses of several adjacent thoracic vertebrae. Their surface is uneven, with deep grooves in the anterior sections. Reactive sclerotic changes are noted around the urinary tract.
Subsequently, there is a delay in the growth of the anterior parts of the vertebral bodies, which acquire a wedge-shaped shape. The intervertebral discs are initially unchanged, but in the subsequent period their height decreases. In the outcome phase, calcification of the anterior longitudinal ligament is observed.
